MYOCARDITIS
BY
Dr. Mahadev Harani
MBBS, M.Phil, FCPS.
Professor Pathology,
LUMHS Jamshoro.
Diverse group of pathologic entities in
 which microorganisms and/or an
 inflammatory process cause myocardial
 injury.
ETIOLOGY
 • Viral
 • Non-viral, Trypanosoma, Trichinosis,
   Toxoplasmosis, Diphtheria.
 • Non-Infectious due to Hypersensitivity
   reactions.
 • Drugs.Antibiotics, Diuretics and anti
   Hypertensive. Also associated with systemic
   diseases of immune origin. RF, SLE,
   polymyositis. Cardiac sarcoidosis and
   rejection of transplanted heart.
MORPHOLOGY
Acute    phase heart may be normal or
 dilated. Some hypertrophy may be present.
In advance stages of disease ventricular
 myocardium is flabby and often mottled
 with minute hemorrhagic lesions.Mural
 thrombi in any chamber.
During active disease myocarditis is mostly
 associated with interstitial inflammatory
 infiltrate associated with focal myocyte
 necrosis.
Continued
 Lymphocytic infiltrate is most common and
 Endomyocardial biopsy is diagnostic.
Lymphocytic myocarditis is most common.
 If the patient survives the acute phase of
 myocarditis, the inflammatory lesions either
 resolve, leaving no residual changes, or heal by
 progressive fibrosis.
Hypersensitivity myocarditis has interstitial
 infiltrate principally perivascular, composed of
 lymphocytes, macrophages and eosinophils.
Giant-cell   myocarditis. characterized by
 widespread inflammatory cellular infiltrates
 containing multinucleate giant cells (formed
 by macrophage fusion) interspersed with
 lymphocytes, eosinophils, and plasma cells.
Myocarditis of chagas disease show
 parasite trypanosomes accompanied by an
 inflammatory infiltrate of neutrophils,
 lymphocytes, macrophages, and occasional
 eosinophils
CLINICAL FEATURES
Asymptomatic,   recover completely.
Symptomatic, heart failure, arrhythmias
 and sudden death.
Symptoms of fatigue, dyspnea, palpitation,
 precordial discomfort and fever.
c/f mimic acute MI.
Occasionaly dilated cardiomyopathy is
 late complication.
Other causes of myocardial disease
Cytotoxic drugs.
Catecholamines, Amyloidosis, Iron over
 load, Hyper and hypothyroidism.
PERICARDIAL DISEASE

Diseases  of the pericardium include
 inflammatory conditions and effusions.
Isolated pericardial disease is unusual, and
 pericardial lesions are almost always
 associated with disease in other portions of
 the heart or surrounding structures, or are
 secondary to a systemic disorder.

1)Fluidaccumulation 2)Inflammation
 3)Fibrous constriction.
Normally fluid 30-50ml thin, clear, strans
 colomned fluid.
Serous  fluid :Pericardial effusion
Blood        :Hemopericardium
Pus           :Purulent Pericarditis
500ml, chronic globular enlargement.
In acute state 200-300ml produce
 compression due to ruptured MI or
 aortic dissection
PERICARDITIS
Inflammation   of pericardium.

Primary     Rare, viral in origin.

Secondary      Due to cardiac diseases,
 thoracic, systemic, metastases, surgical
 procedures.
Causes.
INFECTIVE:
Virus, pyogenic bacteria, TB, Fungi,
 Parasites.

IMMUNOLOGICALLY         MEDICATED:
 RF, SLE, Scleroderma, Drug
 hypersensitivity
 reaction
MISCELLANOUS:
MI, uremia, Neoplasia, Trauma, Radiation
ACUTE PERICARDITIS
Serous    Pericarditis: Produced by non-
 infectious inflammatory disease such as RF,
 SLE, Scleroderma, tumor, uraemia.
Bacterial pleuritis may cause sufficient
 irritation of pericardium.
Viral Infection antedates pericarditis.
MORPHOLOGY: Inflammatory reaction
 with few neutrophils,lymphocytes and
 histiocytes.
Volume  of fluid between 50-200
 ml,accumulates slowly.
Organization into fibrous rarelr occurs.
FIBRINOUS AND SEROFIBRINOUS PERICARDITIS

Serous Fluid mixed with fibrinous exudate.
Common Causes: Acute MI, Dressler
 syndrome, Uraemia, Chest radiation, RF,
 SLE, Trauma.
IN FIBRINOUS PERICARDITIS
The  surface is dry with fine granular
  roughening.
In sero-fibrinous carditis
Intense  inflammatory process, produces
 large amount of yellow to brown fluid
 with presence of leukocytes and red cells
 with fibrin.
Clinically precardial friction rub heard.
Pain, febrile reaction with signs of cardiac
 failure.
Purulent or suppurative Pericarditis
Invasion    of pericardial space by microbes.
a) Direct extension from empyema
b) Seeding from blood
c) Lymphatic extension
d) Direct extension during cardiotomy
Immunosupression pre-disposes to
   infection.
Continued
Exudate  ranges from thin cloudy fluid to
 pus 400-500ml, in volume.
Serosal surface red, granular and coated
 with exudate.
Microscopically acute inflammatory
 reaction seen.
Scarring produce constrictive
 pericarditis.
Signs of systemic infection noticed.
Haemorrhagic Pericarditis
Blood  mixed with fibrinous or suppurative
 effusion due to neoplasm. Cytological
 examination needed.
Also seen in bacterial infection due to
 bleeding diathesis.
Also due to cardiac surgery.
Caseous Pericarditis
Rare,due   to tuberculosis until proved
 other wise.
It leads to chronic constrictive
 pericarditis
U
           Y O
          K
     AN
TH

Pericarditis

  • 1.
    MYOCARDITIS BY Dr. Mahadev Harani MBBS,M.Phil, FCPS. Professor Pathology, LUMHS Jamshoro.
  • 2.
    Diverse group ofpathologic entities in which microorganisms and/or an inflammatory process cause myocardial injury.
  • 3.
    ETIOLOGY • Viral • Non-viral, Trypanosoma, Trichinosis, Toxoplasmosis, Diphtheria. • Non-Infectious due to Hypersensitivity reactions. • Drugs.Antibiotics, Diuretics and anti Hypertensive. Also associated with systemic diseases of immune origin. RF, SLE, polymyositis. Cardiac sarcoidosis and rejection of transplanted heart.
  • 4.
    MORPHOLOGY Acute phase heart may be normal or dilated. Some hypertrophy may be present. In advance stages of disease ventricular myocardium is flabby and often mottled with minute hemorrhagic lesions.Mural thrombi in any chamber. During active disease myocarditis is mostly associated with interstitial inflammatory infiltrate associated with focal myocyte necrosis.
  • 5.
    Continued Lymphocytic infiltrateis most common and Endomyocardial biopsy is diagnostic. Lymphocytic myocarditis is most common. If the patient survives the acute phase of myocarditis, the inflammatory lesions either resolve, leaving no residual changes, or heal by progressive fibrosis. Hypersensitivity myocarditis has interstitial infiltrate principally perivascular, composed of lymphocytes, macrophages and eosinophils.
  • 6.
    Giant-cell myocarditis. characterized by widespread inflammatory cellular infiltrates containing multinucleate giant cells (formed by macrophage fusion) interspersed with lymphocytes, eosinophils, and plasma cells. Myocarditis of chagas disease show parasite trypanosomes accompanied by an inflammatory infiltrate of neutrophils, lymphocytes, macrophages, and occasional eosinophils
  • 7.
    CLINICAL FEATURES Asymptomatic, recover completely. Symptomatic, heart failure, arrhythmias and sudden death. Symptoms of fatigue, dyspnea, palpitation, precordial discomfort and fever. c/f mimic acute MI. Occasionaly dilated cardiomyopathy is late complication.
  • 8.
    Other causes ofmyocardial disease Cytotoxic drugs. Catecholamines, Amyloidosis, Iron over load, Hyper and hypothyroidism.
  • 9.
    PERICARDIAL DISEASE Diseases of the pericardium include inflammatory conditions and effusions. Isolated pericardial disease is unusual, and pericardial lesions are almost always associated with disease in other portions of the heart or surrounding structures, or are secondary to a systemic disorder. 1)Fluidaccumulation 2)Inflammation 3)Fibrous constriction. Normally fluid 30-50ml thin, clear, strans colomned fluid.
  • 10.
    Serous fluid:Pericardial effusion Blood :Hemopericardium Pus :Purulent Pericarditis 500ml, chronic globular enlargement. In acute state 200-300ml produce compression due to ruptured MI or aortic dissection
  • 11.
    PERICARDITIS Inflammation of pericardium. Primary Rare, viral in origin. Secondary Due to cardiac diseases, thoracic, systemic, metastases, surgical procedures.
  • 12.
    Causes. INFECTIVE: Virus, pyogenic bacteria,TB, Fungi, Parasites. IMMUNOLOGICALLY MEDICATED: RF, SLE, Scleroderma, Drug hypersensitivity reaction MISCELLANOUS: MI, uremia, Neoplasia, Trauma, Radiation
  • 13.
    ACUTE PERICARDITIS Serous Pericarditis: Produced by non- infectious inflammatory disease such as RF, SLE, Scleroderma, tumor, uraemia. Bacterial pleuritis may cause sufficient irritation of pericardium. Viral Infection antedates pericarditis. MORPHOLOGY: Inflammatory reaction with few neutrophils,lymphocytes and histiocytes.
  • 14.
    Volume offluid between 50-200 ml,accumulates slowly. Organization into fibrous rarelr occurs.
  • 15.
    FIBRINOUS AND SEROFIBRINOUSPERICARDITIS Serous Fluid mixed with fibrinous exudate. Common Causes: Acute MI, Dressler syndrome, Uraemia, Chest radiation, RF, SLE, Trauma. IN FIBRINOUS PERICARDITIS The surface is dry with fine granular roughening.
  • 16.
    In sero-fibrinous carditis Intense inflammatory process, produces large amount of yellow to brown fluid with presence of leukocytes and red cells with fibrin. Clinically precardial friction rub heard. Pain, febrile reaction with signs of cardiac failure.
  • 17.
    Purulent or suppurativePericarditis Invasion of pericardial space by microbes. a) Direct extension from empyema b) Seeding from blood c) Lymphatic extension d) Direct extension during cardiotomy Immunosupression pre-disposes to infection.
  • 18.
    Continued Exudate rangesfrom thin cloudy fluid to pus 400-500ml, in volume. Serosal surface red, granular and coated with exudate. Microscopically acute inflammatory reaction seen. Scarring produce constrictive pericarditis. Signs of systemic infection noticed.
  • 19.
    Haemorrhagic Pericarditis Blood mixed with fibrinous or suppurative effusion due to neoplasm. Cytological examination needed. Also seen in bacterial infection due to bleeding diathesis. Also due to cardiac surgery.
  • 20.
    Caseous Pericarditis Rare,due to tuberculosis until proved other wise. It leads to chronic constrictive pericarditis
  • 21.
    U Y O K AN TH